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Cap analysis gene analysis (CAGE) of primary AML samples harbouring FLT3-ITD mutation (human)

ABSTRACT: Cap analysis gene analysis (CAGE) of primary AML samples harbouring FLT3-ITD mutation (human)

PROVIDER: PRJNA630702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11711371.fastq.gz	Fastqsanger.gz
	SRR11711372.fastq.gz	Fastqsanger.gz
	SRR11711373.fastq.gz	Fastqsanger.gz
	SRR11711374.fastq.gz	Fastqsanger.gz
	SRR11711375.fastq.gz	Fastqsanger.gz

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Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

Project description:This SuperSeries is composed of the SubSeries listed below. The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML cells (primary samples and Ba/F3 cell) and the underlying molecular mechanism of mutation-driven acquired resistance. We identify 310 upregulated and 22 downregulated promoters in FLT3-ITD/D835 mutant AML cells compared to cells with FLT3-ITD (FDR<0.05), and 1945 upregulated and 1470 downregulated promoters in FLT3-ITD/D835 mutant Ba/F3 cells compared to cells with FLT3-ITD.

2023-05-08 | GSE149964 | GEO

Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

Project description:Cap analysis gene analysis (CAGE) of AML cells harbouring FLT3-ITD mutations

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Cap analysis gene analysis (CAGE) of primary AML samples harbouring FLT3-ITD mutation (human)

Project description:The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML and the underlying molecular mechanism of mutation-driven acquired resistance. We identify that 310 upregulated and 22 downregulated promoters in FLT3-ITD/D835 mutant AML cells compared to cells with FLT3-ITD (FDR<0.05).

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Cap analysis gene analysis (CAGE) of Ba/F3 cells harbouring FLT3-ITD mutations (mouse)

Project description:The purpose of the experiment is to investigate transcriptome signatures of FLT3-ITD and TKD double mutations in AML and the underlying molecular mechanism of mutation-driven acquired resistance. We identify 1945 upregulated and 1470 downregulated promoters in FLT3-ITD/D835 mutant Ba/F4 cells compared to cells with FLT3-ITD (FDR<0.05).

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Cap analysis gene analysis (CAGE) of Ba/F3 cells harbouring FLT3-ITD mutations (mouse)

Project description:Cap analysis gene analysis (CAGE) of Ba/F3 cells harbouring FLT3-ITD mutations (mouse)

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RNA sequencing of MV4;11 cells harbouring FLT3-ITD mutations

Project description:The purpose of the experiment is to investigate whether more co-mutations exists in MV4;11 cells harboring FLT3-ITD/D835 than cells with FLT3-ITD only.

2023-05-27 | GSE151249 | GEO

RNA sequencing of MV4 11 cells harbouring FLT3-ITD mutations

Project description:RNA sequencing of MV4 11 cells harbouring FLT3-ITD mutations

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MS-based phosphoproteomic of cytarabine-treated FLT3-ITD cells

Project description:ITD mutations in the FLT3 gene occur in the 30% of acute myeloid leukemia patients. The integration of ITD in the tyrosine kinase domain (TKD-ITD) of the FLT3 receptor has been shown to confer resistance to standard chemotherapy treatment. We applied state-of-the-art, high-sensitive, mass spectrometry (MS)-based (phospho)proteomics to investigate the molecular mechanisms underlying the sensitivity to cytarabine therapy in FLT3-ITD cells.

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Expression profile of hematopoietic stem and progenitor cell (HSPC) compartment of FLT3-ITD and FLT3-ITD miR-155-/- mice

Project description:The miR-155-dependent differences in gene expression in the HSPC compartment of FLT3-ITD mice is unknown. In this experiment, we performed RNA sequencing on FLT3-ITD and FLT3-ITD miR-155-/- mouse LKS cells.

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CircMYBL2 Regulates FLT3-ITD FLT3AML Translation in AML

Project description:CircMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. We used the ribosome profiling and RNA-seq libraries sequenced with Illumina HiSeq 2500 to identify the mRNA that circMYBL2 targeted. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. Mechanistically, circMYBL2 enhanced the translational efficiency of FLT3 kinase by increasing the binding of PTBP1 to FLT3 mRNA. Moreover, circMYBL2 knockdown impaired the cytoactivity of inhibitor-resistant FLT3-ITD-positive cells, with a significant decrease in FLT3 kinase expression, followed by the inactivation of its downstream pathways. In summary, we are the first to reveal a circRNA that specifically influences FLT3-ITD AML and regulates FLT3 kinase levels through translational regulation, suggesting that circMYBL2 may be a potential therapeutic target for FLT3-ITD AML.

2019-07-09 | GSE133925 | GEO

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